This document discusses the approach to evaluating and treating narrow complex tachycardia. It begins by describing the different mechanisms of tachyarrhythmias including enhanced automaticity, triggered automaticity, and reentry. It then discusses specific types of narrow complex tachycardia such as AV nodal reentrant tachycardia, AV reentrant tachycardia, atrial tachycardia, junctional ectopic tachycardia, and atrial flutter. It provides guidance on evaluating the ECG and patient response to determine the mechanism and appropriate treatment. Treatment options discussed include vagal maneuvers, adenosine, calcium channel blockers, beta blockers, and cardioversion for unstable patients.
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Atrial flutter is a reentrant tachycardia involving the right atrium. There are two main types - typical atrial flutter which revolves counterclockwise around the tricuspid annulus, and reverse typical atrial flutter which revolves clockwise. Catheter ablation aims to create a continuous linear lesion across the cavotricuspid isthmus to block conduction and terminate the arrhythmia. Successful ablation is confirmed by the inability to induce flutter and demonstration of bidirectional conduction block across the ablation line.
1) The document defines wide complex tachycardia as a rhythm with a QRS duration ≥120ms and heart rate >100 bpm.
2) The main causes listed are ventricular tachycardia (80% of cases) and supraventricular tachycardia with aberrancy.
3) Key features that can help differentiate the underlying rhythm include QRS duration, axis, morphology, and the presence or absence of AV dissociation on electrocardiogram.
The Long QT Syndrome: Overview and Management The Long QT Syndrome: Overvie...MedicineAndFamily
Long QT Syndrome is a genetic disorder characterized by a prolonged QT interval on electrocardiogram that can cause dangerous arrhythmias and sudden cardiac death. Symptoms include unexplained fainting, seizures, or sudden death, especially with exercise or emotions. Treatment involves beta blockers, implantable cardioverter defibrillators, or left stellate ganglionectomy depending on risk level and genotype. Ongoing research seeks to better understand genotype-phenotype relationships and develop mutation-specific therapies.
Wide complex Tachycardia by Dr. Vaibhav Yawalkarvaibhavyawalkar
This document discusses wide QRS complex tachycardia, including definitions, causes, and approaches to distinguishing supraventricular tachycardia (SVT) from ventricular tachycardia (VT). Key points include: SVT accounts for 20% of cases while VT accounts for 80%; maneuvers like carotid sinus pressure may help identify SVT that terminates in response; ECG criteria like axis, concordance, AV dissociation, and QRS morphology provide clues but are imperfect; treatment should initially treat any wide QRS tachycardia as VT due to risk of incorrectly treating SVT as VT. Distinguishing the arrhythmia is important but difficult, so the document reviews multiple diagnostic algorithms and criteria to
This document discusses wide complex tachycardia (WCT), which is ventricular in origin 80% of the time. In patients with structural heart disease, 95% of WCT is ventricular tachycardia (VT). VT can be life-threatening and cause sudden death or tachycardia-induced cardiomyopathy. The document describes types of VT based on morphology and duration, symptoms of VT, features that appear on ECGs during VT like abnormal wide QRS complexes and AV dissociation, and examples of patients presenting with potential VT.
This document discusses localization of accessory pathways using electrocardiography. It describes that accessory pathways can be located in eight anatomical positions along the tricuspid and mitral valve annuli. Several algorithms are proposed to determine the location based on delta wave polarity and amplitude in various leads. The most accurate is the Arruda approach, which uses step-wise analysis of delta wave characteristics in leads I, II, aVL, aVF and V1 to identify the specific accessory pathway location with 90% sensitivity and 99% specificity. Characteristic ECG patterns are presented that help localize right anteroseptal, right posteroseptal, left lateral and right free wall accessory pathways.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy. The document outlines the following approach:
1. Obtain history, physical exam, and 12-lead electrocardiogram (ECG) findings to help determine VT vs SVT. Features like AV dissociation or axis deviation favor VT.
2. Use criteria/algorithms like Wellens, Brugada, Vereckei (incorporating lead aVR) to analyze ECG morphology. A majority of criteria must be met to diagnose VT.
3. Consider electrophysiological testing like measuring His-ventricular intervals
Tachycardias are broadly categorized based upon the width of the QRS complex on the electrocardiogram (ECG). A narrow QRS complex (<120 milliseconds) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia). The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites. A widened QRS (≥120 milliseconds) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia). Alternatively, a supraventricular arrhythmia can produce a widened QRS if there are either pre-existing or rate-related abnormalities within the His-Purkinje system (eg, supraventricular tachycardia with aberrancy), or if conduction occurs over an accessory pathway. Thus, wide QRS complex tachycardias may be either supraventricular or ventricular in origin.
Atrial flutter is a reentrant tachycardia involving the right atrium. There are two main types - typical atrial flutter which revolves counterclockwise around the tricuspid annulus, and reverse typical atrial flutter which revolves clockwise. Catheter ablation aims to create a continuous linear lesion across the cavotricuspid isthmus to block conduction and terminate the arrhythmia. Successful ablation is confirmed by the inability to induce flutter and demonstration of bidirectional conduction block across the ablation line.
1) The document defines wide complex tachycardia as a rhythm with a QRS duration ≥120ms and heart rate >100 bpm.
2) The main causes listed are ventricular tachycardia (80% of cases) and supraventricular tachycardia with aberrancy.
3) Key features that can help differentiate the underlying rhythm include QRS duration, axis, morphology, and the presence or absence of AV dissociation on electrocardiogram.
The Long QT Syndrome: Overview and Management The Long QT Syndrome: Overvie...MedicineAndFamily
Long QT Syndrome is a genetic disorder characterized by a prolonged QT interval on electrocardiogram that can cause dangerous arrhythmias and sudden cardiac death. Symptoms include unexplained fainting, seizures, or sudden death, especially with exercise or emotions. Treatment involves beta blockers, implantable cardioverter defibrillators, or left stellate ganglionectomy depending on risk level and genotype. Ongoing research seeks to better understand genotype-phenotype relationships and develop mutation-specific therapies.
Wide complex Tachycardia by Dr. Vaibhav Yawalkarvaibhavyawalkar
This document discusses wide QRS complex tachycardia, including definitions, causes, and approaches to distinguishing supraventricular tachycardia (SVT) from ventricular tachycardia (VT). Key points include: SVT accounts for 20% of cases while VT accounts for 80%; maneuvers like carotid sinus pressure may help identify SVT that terminates in response; ECG criteria like axis, concordance, AV dissociation, and QRS morphology provide clues but are imperfect; treatment should initially treat any wide QRS tachycardia as VT due to risk of incorrectly treating SVT as VT. Distinguishing the arrhythmia is important but difficult, so the document reviews multiple diagnostic algorithms and criteria to
This document discusses wide complex tachycardia (WCT), which is ventricular in origin 80% of the time. In patients with structural heart disease, 95% of WCT is ventricular tachycardia (VT). VT can be life-threatening and cause sudden death or tachycardia-induced cardiomyopathy. The document describes types of VT based on morphology and duration, symptoms of VT, features that appear on ECGs during VT like abnormal wide QRS complexes and AV dissociation, and examples of patients presenting with potential VT.
This document discusses localization of accessory pathways using electrocardiography. It describes that accessory pathways can be located in eight anatomical positions along the tricuspid and mitral valve annuli. Several algorithms are proposed to determine the location based on delta wave polarity and amplitude in various leads. The most accurate is the Arruda approach, which uses step-wise analysis of delta wave characteristics in leads I, II, aVL, aVF and V1 to identify the specific accessory pathway location with 90% sensitivity and 99% specificity. Characteristic ECG patterns are presented that help localize right anteroseptal, right posteroseptal, left lateral and right free wall accessory pathways.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy. The document outlines the following approach:
1. Obtain history, physical exam, and 12-lead electrocardiogram (ECG) findings to help determine VT vs SVT. Features like AV dissociation or axis deviation favor VT.
2. Use criteria/algorithms like Wellens, Brugada, Vereckei (incorporating lead aVR) to analyze ECG morphology. A majority of criteria must be met to diagnose VT.
3. Consider electrophysiological testing like measuring His-ventricular intervals
The document discusses various electrocardiogram (ECG) criteria for differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy presenting with a wide QRS complex tachycardia. It outlines criteria from Sandler and Marriott (1965), Wellens (1978), Kindwall (1988), Brugada (1991), Vereckei (2008) and Pava (2010). Key criteria that favor VT include QRS duration >140ms, extreme left axis, AV dissociation, monophasic R wave in V1, R/S ratio <1 in V6, and notching of the S wave in V1.
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
This document provides information on various types of supraventricular tachyarrhythmias including AV nodal reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT), atrial tachycardia, junctional tachycardias, Wolff-Parkinson-White (WPW) syndrome, and atrial fibrillation. It discusses the mechanisms, ECG patterns, symptoms, diagnostic approaches, and management options for these arrhythmias in 1-3 sentences per type of arrhythmia.
Ventricular tachycardia can occur in structurally normal hearts. It is classified based on origin, morphology, response to exercise and drugs. Non-life threatening VT is often monomorphic and originates from sites like outflow tracts and fascicles. Outflow tract VT commonly originates from the right ventricular outflow tract. Other sites include the left ventricular outflow tract and aortic cusps. Treatment includes medications, ablation, and implantable cardioverter-defibrillators for more severe cases. Life-threatening VT is often polymorphic and associated with genetic ion channel disorders like long QT syndrome.
The document discusses various types of arrhythmias and their mechanisms. It describes ectopic beats that originate from locations other than the sinoatrial node, and explains that they can cause single beats or take over the heart rhythm. The mechanisms of arrhythmias include altered automaticity, triggered activity, and reentry. Reentry involves unidirectional block and different conduction speeds that allow an impulse to circulate and repeat, creating a reentrant circuit. The document outlines several specific types of arrhythmias like atrial fibrillation, atrial flutter, atrioventricular nodal reentry, and Wolff-Parkinson-White syndrome.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
This document provides an overview of echocardiographic evaluation of restrictive cardiomyopathy. Key points include:
- Restrictive cardiomyopathy is characterized by a nondilated left ventricle with abnormal diastolic function and typically normal systolic function.
- Causes include infiltrative diseases like amyloidosis and storage diseases. Echocardiography can help diagnose but it is more difficult than other cardiomyopathies.
- Findings include low diastolic volume, normal ejection fraction, diastolic dysfunction with rapid early mitral inflow. Echocardiography helps differentiate restrictive cardiomyopathy from constrictive pericarditis.
The document discusses Long QT Syndrome (LQTS), an inherited heart condition characterized by an abnormally prolonged QT interval on electrocardiograms. It describes the causes and types of LQTS, including LQT1, LQT2 and LQT3, which are associated with different genetic mutations and ECG patterns. The main symptoms of LQTS are syncope and cardiac arrest, typically in children or teenagers. Diagnosis involves measuring the QT interval and identifying risk factors. Treatment focuses on beta-blockers, lifestyle changes and implantable cardioverter-defibrillators for high-risk patients.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia with aberrancy (SVT-A). The document discusses various algorithms and criteria for making this distinction using the electrocardiogram. These include Wellens' criteria, Brugada criteria, Vereckei's aVR algorithm, and analyzing features such as QRS morphology and the presence of atrioventricular dissociation. No single algorithm is perfect, so electrophysiological testing may be needed in some cases to make a definitive diagnosis and guide appropriate treatment.
This document discusses algorithms and ECG parameters for differentiating between types of narrow complex tachycardia, including atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Key parameters discussed include the presence of pseudo waves, retrograde P wave morphology and position, and the RP interval. The Jaeggi algorithm uses these parameters to differentiate AVNRT from AVRT based on ECG analysis alone in 76% of cases. Retrograde P wave morphology varies depending on the location of the accessory pathway in cases of AVRT.
The document provides an overview of electrocardiography (ECG) interpretation. It discusses the heart's electrical conduction system and action potential, as well as the basics of reading an ECG including assessing rhythm, rate, axis, P waves, QRS complex, ST segment, and T waves. It outlines common abnormalities and provides examples of ECG interpretations for case scenarios involving myocardial infarction, left ventricular hypertrophy, sinus arrhythmia, and atrial fibrillation. The goal is to teach readers how to systematically evaluate an ECG tracing and identify potential cardiac issues.
This document discusses wide complex tachycardias and how to differentiate them based on electrocardiogram (ECG) findings. It provides details on what makes a complex narrow or wide, types of wide complex tachycardias including ventricular tachycardia and supraventricular tachycardia, and ECG criteria to help determine the source and mechanism such as the presence or absence of RS complexes and their intervals. Morphologic criteria on the ECG and algorithms like the ACC algorithm are presented to aid in differential diagnosis.
This document provides an overview of the approach to evaluating and diagnosing wide complex tachycardias. It begins with definitions of terms like wide complex tachycardia, ventricular tachycardia, and supraventricular tachycardia. It then discusses the importance of making an accurate diagnosis to avoid inappropriate treatment. Various ECG criteria are presented to help distinguish ventricular from supraventricular rhythms based on features like AV dissociation, QRS morphology, axis, and precordial patterns. Specific criteria for right bundle branch block and left bundle branch block morphologies are also outlined. The document emphasizes taking a stepwise approach and considering clinical history in narrowing the differential diagnosis of wide complex tachycardias.
1) Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia. It involves a reentrant circuit utilizing the fast and slow pathways within the AV node.
2) There are typical and atypical forms of AVNRT depending on the direction of conduction through the fast and slow pathways. In typical AVNRT, antegrade conduction is down the slow pathway and retrograde up the fast pathway. In atypical AVNRT the directions are reversed.
3) Ablation of the slow pathway is an effective treatment for AVNRT and can be performed without damaging the AV node since only a portion of the circuit
This document describes different types of supraventricular tachycardias (SVTs), which are rapid heart rhythms originating above the ventricles. It defines SVTs and paroxysmal supraventricular tachycardia (PSVT), and lists common symptoms. The types of SVTs are categorized based on their origin in the sinoatrial node, atria, or atrioventricular node/junction. Each type has a distinct electrocardiogram appearance and cause, such as reentry circuits, ectopic foci, or increased node automaticity. Common examples include AV nodal reentrant tachycardia, atrial fibrillation, atrial flutter, and Wolff-Parkinson-
This document contains a quiz with multiple choice questions about ECG interpretations. Some key findings included in the questions are right bundle branch block with left posterior hemiblock, third degree atrioventricular block, left bundle branch block with Cabrera's sign indicating possible myocardial infarction, Wolff-Parkinson-White syndrome type A, ventricular tachycardia, atrial fibrillation, premature ventricular contractions, left ventricular hypertrophy, anterior myocardial infarction, hyperkalemia, and more. The document also includes explanations of ECG patterns and signs such as bundle branch blocks, ventricular tachycardia criteria, Wellens' phenomenon, hyperacute T waves, and more.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
This document discusses techniques for localizing the site of origin of ventricular tachycardia based on electrocardiogram characteristics. It describes that right ventricular outflow tract tachycardias typically present with left bundle branch block morphology while left ventricular sites may present with either right or left bundle branch block depending on exit site. Specific leads are discussed that can provide clues about anterior vs posterior, septal vs free wall origin within the outflow tracts. Other areas like fascicles, papillary muscles and mitral/tricuspid annuli are also summarized.
1. This document discusses the approach to evaluating and diagnosing narrow complex tachycardias. It describes the main mechanisms that can cause tachycardias including enhanced automaticity, triggered activity, and reentry.
2. Specific tachycardia types are then discussed in detail including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), and inappropriate sinus tachycardia. The diagnostic criteria and distinguishing characteristics of each are provided.
3. A number of other arrhythmias are also briefly covered such
1. Tachyarrhythmias are abnormal heart rhythms with a rate over 100 beats per minute. They can originate from the atria, AV node, or ventricles.
2. Common supraventricular tachycardias include sinus tachycardia, atrial fibrillation, atrial flutter, and AV nodal reentrant tachycardia. Atrial fibrillation is characterized by irregularly irregular rhythm without P waves.
3. Ventricular arrhythmias include premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation. Polymorphic ventricular tachycardia can degenerate into ventricular fibrillation and requires immediate defibrillation.
The document discusses various electrocardiogram (ECG) criteria for differentiating between ventricular tachycardia (VT) and supraventricular tachycardia (SVT) with aberrancy presenting with a wide QRS complex tachycardia. It outlines criteria from Sandler and Marriott (1965), Wellens (1978), Kindwall (1988), Brugada (1991), Vereckei (2008) and Pava (2010). Key criteria that favor VT include QRS duration >140ms, extreme left axis, AV dissociation, monophasic R wave in V1, R/S ratio <1 in V6, and notching of the S wave in V1.
A 73-year-old male presented with dizziness for 1 year and chest pain for 2 days. His ECG showed left bundle branch block (LBBB) and first-degree atrioventricular block, consistent with possible trifascicular block. Trifascicular block must be confirmed with bundle of His electrogram. The patient has abnormal conduction through one or more divisions of the intraventricular conduction system distal to the bundle of His, presenting as LBBB and first-degree AV block. This suggests involvement of the left and right bundles as well as the AV node, consistent with trifascicular block.
This document provides information on various types of supraventricular tachyarrhythmias including AV nodal reentrant tachycardia (AVNRT), orthodromic reciprocating tachycardia (ORT), atrial tachycardia, junctional tachycardias, Wolff-Parkinson-White (WPW) syndrome, and atrial fibrillation. It discusses the mechanisms, ECG patterns, symptoms, diagnostic approaches, and management options for these arrhythmias in 1-3 sentences per type of arrhythmia.
Ventricular tachycardia can occur in structurally normal hearts. It is classified based on origin, morphology, response to exercise and drugs. Non-life threatening VT is often monomorphic and originates from sites like outflow tracts and fascicles. Outflow tract VT commonly originates from the right ventricular outflow tract. Other sites include the left ventricular outflow tract and aortic cusps. Treatment includes medications, ablation, and implantable cardioverter-defibrillators for more severe cases. Life-threatening VT is often polymorphic and associated with genetic ion channel disorders like long QT syndrome.
The document discusses various types of arrhythmias and their mechanisms. It describes ectopic beats that originate from locations other than the sinoatrial node, and explains that they can cause single beats or take over the heart rhythm. The mechanisms of arrhythmias include altered automaticity, triggered activity, and reentry. Reentry involves unidirectional block and different conduction speeds that allow an impulse to circulate and repeat, creating a reentrant circuit. The document outlines several specific types of arrhythmias like atrial fibrillation, atrial flutter, atrioventricular nodal reentry, and Wolff-Parkinson-White syndrome.
Ventricular tachycardia can occur due to various causes like acute myocardial infarction, chronic infarction, dilated cardiomyopathy, etc. It is classified as sustained, non-sustained, monomorphic, polymorphic, etc. based on characteristics. Diagnosis involves ECG, echocardiogram, and monitoring. Treatment depends on hemodynamic stability and includes electrical cardioversion, antiarrhythmic drugs like amiodarone, lidocaine, ablation, and ICD implantation in selected cases. Recurrence risk is high in structurally abnormal hearts and prevention involves controlling triggers, antiarrhythmics, and ICDs.
This document provides an overview of echocardiographic evaluation of restrictive cardiomyopathy. Key points include:
- Restrictive cardiomyopathy is characterized by a nondilated left ventricle with abnormal diastolic function and typically normal systolic function.
- Causes include infiltrative diseases like amyloidosis and storage diseases. Echocardiography can help diagnose but it is more difficult than other cardiomyopathies.
- Findings include low diastolic volume, normal ejection fraction, diastolic dysfunction with rapid early mitral inflow. Echocardiography helps differentiate restrictive cardiomyopathy from constrictive pericarditis.
The document discusses Long QT Syndrome (LQTS), an inherited heart condition characterized by an abnormally prolonged QT interval on electrocardiograms. It describes the causes and types of LQTS, including LQT1, LQT2 and LQT3, which are associated with different genetic mutations and ECG patterns. The main symptoms of LQTS are syncope and cardiac arrest, typically in children or teenagers. Diagnosis involves measuring the QT interval and identifying risk factors. Treatment focuses on beta-blockers, lifestyle changes and implantable cardioverter-defibrillators for high-risk patients.
Wide QRS tachycardia requires differentiating between ventricular tachycardia (VT) and supraventricular tachycardia with aberrancy (SVT-A). The document discusses various algorithms and criteria for making this distinction using the electrocardiogram. These include Wellens' criteria, Brugada criteria, Vereckei's aVR algorithm, and analyzing features such as QRS morphology and the presence of atrioventricular dissociation. No single algorithm is perfect, so electrophysiological testing may be needed in some cases to make a definitive diagnosis and guide appropriate treatment.
This document discusses algorithms and ECG parameters for differentiating between types of narrow complex tachycardia, including atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT). Key parameters discussed include the presence of pseudo waves, retrograde P wave morphology and position, and the RP interval. The Jaeggi algorithm uses these parameters to differentiate AVNRT from AVRT based on ECG analysis alone in 76% of cases. Retrograde P wave morphology varies depending on the location of the accessory pathway in cases of AVRT.
The document provides an overview of electrocardiography (ECG) interpretation. It discusses the heart's electrical conduction system and action potential, as well as the basics of reading an ECG including assessing rhythm, rate, axis, P waves, QRS complex, ST segment, and T waves. It outlines common abnormalities and provides examples of ECG interpretations for case scenarios involving myocardial infarction, left ventricular hypertrophy, sinus arrhythmia, and atrial fibrillation. The goal is to teach readers how to systematically evaluate an ECG tracing and identify potential cardiac issues.
This document discusses wide complex tachycardias and how to differentiate them based on electrocardiogram (ECG) findings. It provides details on what makes a complex narrow or wide, types of wide complex tachycardias including ventricular tachycardia and supraventricular tachycardia, and ECG criteria to help determine the source and mechanism such as the presence or absence of RS complexes and their intervals. Morphologic criteria on the ECG and algorithms like the ACC algorithm are presented to aid in differential diagnosis.
This document provides an overview of the approach to evaluating and diagnosing wide complex tachycardias. It begins with definitions of terms like wide complex tachycardia, ventricular tachycardia, and supraventricular tachycardia. It then discusses the importance of making an accurate diagnosis to avoid inappropriate treatment. Various ECG criteria are presented to help distinguish ventricular from supraventricular rhythms based on features like AV dissociation, QRS morphology, axis, and precordial patterns. Specific criteria for right bundle branch block and left bundle branch block morphologies are also outlined. The document emphasizes taking a stepwise approach and considering clinical history in narrowing the differential diagnosis of wide complex tachycardias.
1) Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common type of supraventricular tachycardia. It involves a reentrant circuit utilizing the fast and slow pathways within the AV node.
2) There are typical and atypical forms of AVNRT depending on the direction of conduction through the fast and slow pathways. In typical AVNRT, antegrade conduction is down the slow pathway and retrograde up the fast pathway. In atypical AVNRT the directions are reversed.
3) Ablation of the slow pathway is an effective treatment for AVNRT and can be performed without damaging the AV node since only a portion of the circuit
This document describes different types of supraventricular tachycardias (SVTs), which are rapid heart rhythms originating above the ventricles. It defines SVTs and paroxysmal supraventricular tachycardia (PSVT), and lists common symptoms. The types of SVTs are categorized based on their origin in the sinoatrial node, atria, or atrioventricular node/junction. Each type has a distinct electrocardiogram appearance and cause, such as reentry circuits, ectopic foci, or increased node automaticity. Common examples include AV nodal reentrant tachycardia, atrial fibrillation, atrial flutter, and Wolff-Parkinson-
This document contains a quiz with multiple choice questions about ECG interpretations. Some key findings included in the questions are right bundle branch block with left posterior hemiblock, third degree atrioventricular block, left bundle branch block with Cabrera's sign indicating possible myocardial infarction, Wolff-Parkinson-White syndrome type A, ventricular tachycardia, atrial fibrillation, premature ventricular contractions, left ventricular hypertrophy, anterior myocardial infarction, hyperkalemia, and more. The document also includes explanations of ECG patterns and signs such as bundle branch blocks, ventricular tachycardia criteria, Wellens' phenomenon, hyperacute T waves, and more.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
This document discusses techniques for localizing the site of origin of ventricular tachycardia based on electrocardiogram characteristics. It describes that right ventricular outflow tract tachycardias typically present with left bundle branch block morphology while left ventricular sites may present with either right or left bundle branch block depending on exit site. Specific leads are discussed that can provide clues about anterior vs posterior, septal vs free wall origin within the outflow tracts. Other areas like fascicles, papillary muscles and mitral/tricuspid annuli are also summarized.
1. This document discusses the approach to evaluating and diagnosing narrow complex tachycardias. It describes the main mechanisms that can cause tachycardias including enhanced automaticity, triggered activity, and reentry.
2. Specific tachycardia types are then discussed in detail including AV nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), and inappropriate sinus tachycardia. The diagnostic criteria and distinguishing characteristics of each are provided.
3. A number of other arrhythmias are also briefly covered such
1. Tachyarrhythmias are abnormal heart rhythms with a rate over 100 beats per minute. They can originate from the atria, AV node, or ventricles.
2. Common supraventricular tachycardias include sinus tachycardia, atrial fibrillation, atrial flutter, and AV nodal reentrant tachycardia. Atrial fibrillation is characterized by irregularly irregular rhythm without P waves.
3. Ventricular arrhythmias include premature ventricular complexes, ventricular tachycardia, and ventricular fibrillation. Polymorphic ventricular tachycardia can degenerate into ventricular fibrillation and requires immediate defibrillation.
1) Atrial tachycardias can be focal, triggered, or reentrant and include both macroreentrant circuits and focal mechanisms. Sinus node reentry is considered a specific type of focal atrial tachycardia.
2) AV nodal reentrant tachycardia (AVNRT) is a common form of reentrant tachycardia that involves dual pathways in the AV node - a fast and slow pathway. Typical AVNRT uses the slow pathway anterograde and fast pathway retrograde.
3) Other reentrant tachycardias discussed include atypical AVNRT variants, orthodromic and antidromic AV reentrant
1. AVNRT and AVRT are types of supraventricular tachycardia involving abnormal pathways for electrical conduction between the atria and ventricles.
2. AVNRT is caused by a reentry circuit within the AV node, while AVRT involves an accessory pathway bypassing the AV node.
3. There are different subtypes of AVNRT and AVRT depending on which pathways are involved in the antegrade and retrograde directions. Typical AVNRT involves a slow-fast pathway while typical AVRT involves orthodromic conduction over an accessory pathway.
This document discusses various types of arrhythmias including their mechanisms, diagnosis using electrophysiologic studies, and management. It covers topics such as AV nodal reentrant tachycardia, orthodromic reciprocating tachycardia, atrial flutter, atrial tachycardia, Wolff-Parkinson-White syndrome, and differentiation of arrhythmias using pacing techniques during electrophysiology studies. The role of EPS in establishing mechanisms of arrhythmias and guiding treatment is emphasized.
This document discusses approaches to narrow complex tachycardia. It begins by defining narrow QRS tachycardia as having a QRS width of less than 120ms. It then classifies different types of narrow complex tachycardia by site of origin and regularity, including sinus tachycardia, inappropriate sinus tachycardia, sinus node reentrant tachycardia, atrial tachycardia, atrial flutter, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT). It provides details on electrocardiogram features and diagnostic approaches for each type.
The document discusses various types of arrhythmias that may occur during anesthesia including narrow and broad complex arrhythmias. It defines arrhythmia and outlines the conduction pathways in the heart. For narrow complex arrhythmias it describes sinus arrhythmias, premature atrial contractions, sinus bradycardia, sinus tachycardia, junctional tachycardia, atrial flutter and fibrillation. For broad complex arrhythmias it covers ventricular ectopy, ventricular tachycardia and fibrillation. Management strategies are provided for selected arrhythmias.
A 45-year-old female presented with difficulty breathing, palpitations, and sweating for 4 hours. An ECG showed Wolff-Parkinson-White (WPW) syndrome, characterized by a short PR interval, delta wave, and widened QRS complex. WPW is a congenital condition involving an accessory pathway that allows supraventricular impulses to bypass the AV node and activate the ventricles early. Treatment options include antiarrhythmic drugs or radiofrequency ablation to destroy the accessory pathway.
Its crucial to diagnose arrythmias quickly and treat it promptly.
Here i have made small attempt to diagnose tachyarrythmias briefly and proceeds with its immediate managenent..
This document summarizes various cardiac arrhythmias including supraventricular arrhythmias like premature atrial complexes, atrial fibrillation, and atrial flutter as well as ventricular arrhythmias such as premature ventricular complexes and ventricular tachycardia. For each arrhythmia, it describes the characteristic ECG patterns including P wave morphology, QRS width, and rhythm irregularity. It also discusses distinguishing features, causes, and clinical implications of different arrhythmias.
1) AVNRT is the most common cause of palpitations in structurally normal hearts. It involves a reentry circuit within the AV node.
2) The most common type is slow-fast AVNRT, accounting for 80-90% of cases. It involves the slow pathway for anterograde conduction and fast pathway for retrograde conduction.
3) ECG features include a regular narrow-complex tachycardia between 140-280 bpm. P waves may be obscured or visible as pseudo R/S waves depending on the type of AVNRT.
This document discusses various types of cardiac arrhythmias including their mechanisms, ECG features, and treatment approaches. It covers basics of the cardiac action potential and mechanisms that can generate arrhythmias such as accelerated automaticity, triggered activity, and reentry. Specific arrhythmias summarized include:
- Supraventricular tachycardias like sinus tachycardia, AV nodal reentrant tachycardia, AV reciprocating tachycardia, atrial fibrillation, and atrial flutter.
- Ventricular arrhythmias including ventricular tachycardia, ventricular fibrillation, and torsades de pointes.
- Causes, diagnostic ECG patterns,
This document discusses cardiac arrhythmias including their mechanisms and types. It describes the cardiac action potential and how impulses are conducted regularly through the heart. The main types of arrhythmia are defined as bradycardia which is a slow heart rate, and tachycardia which is a fast heart rate. The mechanisms that can generate arrhythmias include accelerated automaticity, triggered activity, and reentry. Specific types of supraventricular tachycardias such as atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardia are then explained in detail.
The document describes several types of normal and abnormal cardiac rhythms as identified by an electrocardiogram (EKG or ECG). It provides descriptions and EKG criteria for normal sinus rhythm, sinus bradycardia, sinus tachycardia, premature atrial complexes, atrial fibrillation, atrial flutter, supraventricular tachycardia, premature junctional complexes, junctional rhythm, various degrees of atrioventricular block, premature ventricular contractions, ventricular bigeminy, and ventricular tachycardia.
This document discusses supraventricular tachycardias (SVT). It defines different types of SVT including paroxysmal SVT, which is common in emergency rooms. Quality of life is often poor for those with paroxysmal SVT. The document discusses mechanisms of SVT including reentry circuits, enhanced automaticity, and triggered activity. It provides details on differentiating AV nodal reentrant tachycardia from AV reentrant tachycardia using electrocardiogram findings. Treatment options discussed include carotid sinus massage, adenosine, and catheter ablation.
Cardiac arrhythmias are abnormalities in the heart's rhythm. There are two main types: bradycardia, a slow heart rate, and tachycardia, a fast heart rate. Various arrhythmias are described including sinus bradycardia, heart block, atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, ventricular fibrillation, and ventricular tachycardia. Treatment depends on the type of arrhythmia and may include medication, cardioversion, ablation, or pacemaker implantation. Diagnosis involves ECG, echocardiogram, blood tests, and other cardiac tests. Lifestyle changes and avoiding arrhythmia triggers can help management.
This document provides an overview of various tachyarrhythmias including their conduction pathways, pathophysiology, ECG characteristics, and treatment approaches. Key points covered include:
- The conduction system of the heart and action potentials across cardiac tissues.
- Causes of tachyarrhythmias including increased automaticity, triggered activity, and reentry.
- Algorithm for evaluating and treating stable vs. unstable tachyarrhythmias.
- Characteristics and management of common tachyarrhythmias like atrial fibrillation, atrial flutter, AV nodal reentrant tachycardia, and ventricular tachycardia.
- Use of synchronized cardioversion for unstable rhythms
This document provides an overview of cardiac arrhythmias, including definitions and descriptions of normal sinus rhythm and various arrhythmias. It discusses the cardiac conduction system and mechanisms that can cause arrhythmias, such as abnormal impulse formation or conduction. Specific arrhythmias summarized include sinus bradycardia, sinus tachycardia, premature atrial contractions, supraventricular tachycardia, atrial fibrillation, atrial flutter, and atrial tachycardia. For each arrhythmia, the document provides information on heart rate, rhythm, P wave presence/morphology, and other ECG characteristics.
This document discusses antiarrhythmic drug therapy and summarizes the following key points:
- Antiarrhythmic drugs are classified into four classes based on their mechanism of action and effects on the cardiac action potential. Classes I-III work by blocking sodium, calcium or potassium channels.
- Class I drugs like quinidine and procainamide work by blocking fast sodium channels, reducing the rate of depolarization. Class II drugs like propranolol are beta blockers that reduce heart rate and conduction velocity.
- Common arrhythmias treated include atrial fibrillation, ventricular tachycardia, and supraventricular tachycardias. Drug choice is based on the arrhythmia type
1. The document describes various types of narrow complex tachycardia (NCT), including atrial fibrillation, atrial flutter, multifocal atrial tachycardia, atrial tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT).
2. Key aspects that help differentiate the NCTs include the presence or absence of P waves, regularity of the rhythm, P wave morphology, and the RP and PR intervals.
3. Aspects like an irregular rhythm with no P waves indicate atrial fibrillation, while regular rhythms with varying
Similar to approach to narrow comlex tachycardia (20)
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
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5. TACHYARRYTHMIAS:
Any disturbance in the normal sequence of impulse generation,
conduction or both in the heart.
Tachyarrhythmias can be classified according to mechanism,
including
1.Enhanced automaticity (spontaneous depolarization of atrial,
junctional, or ventricular pacemakers)
2.Triggered automaticity (initiated by after depolarizations)
occurring during or immediately after cardiac repolarization,
during phase 3 or 4 of the action potential.
3. Reentry (circus propagation of a depolarizing wavefront).
6.
7.
8.
9.
10.
11.
12. Enhanced cardiac automaticity refers to the accelerated
generation of an action potential by either normal pacemaker
tissue (enhanced normal automaticity) or by abnormal tissue
within the myocardium (abnormal automaticity).
The discharge rate of normal or abnormal pacemakers may be
accelerated by drugs, various forms of cardiac disease,
reduction in extracellular potassium, or alterations of autonomic
nervous system tone.
Enhanced normal automaticity accounts for the occurrence of
sinus tachycardia, while abnormal automaticity may result in
various atrial or ventricular arrhythmias, for example, an
accelerated idioventricular rhythm or an ectopic atrial
tachycardia.
Abnormality in impulse formation:
13. An increase in automaticity normally causes
an increase in sinus rate and sinus tachycardia.
Abnormal automaticity is due to an increase in
the slope of phase 4 depolarization in
myocardium or reduced threshold for action
potential depolarization in myocardium other
than the sinus node. Abnormal automaticity
is thought to be responsible for most atrial
premature complexes (APC) and VPCs.
14. Less commonly, abnormal impulse formation is due to
the development of triggered activity.
Triggered activity is related to cellular afterdepolarization
that occur at the end of the action potential, during
phase 3, and are referred to as early afterdepolarization,
or they occur after the action potential, during phase 4,
and are referred to as late afterdepolarization.
15. ABNORMALITY IN IMPULSE PROPAGATION:
The most common arrhythmia mechanism is reentry.
Reentry is defined as circulation of an activation wave
around an inexcitable obstacle. Thus, the requirements
for reentry are two electrophysiologically dissimilar
pathways for impulse propagation around an inexcitable
region such electrophysiologically dissimilar pathways
for impulse propagation around an inexcitable region
such that unidirectional block occurs in one of the
pathways and a region of excitable tissue exists at the
head of the propagating wavefront .
16.
17. Look for QRS duration.
QRS complex regular/irregular.
Then look for presence of p waves.
P waves morphology
P wavesand QRS relationship 1:1
AV block present.
QRS alternation
Termination initiation of tachycardia.
Effect of BBB on tachycardia cycle length.
18.
19.
20. Response to carotid sinus massage or adenosine –with
termination of arrhythmia with Pwave –AVNRT with atrial
premature beat .
Tachycardia persists with AV block –AT, AFL, SANRT
Pseudo r ‘ wave in V1 – AVNRT
SHORT RP interval – AVNRT, AVRT
Long RP interval – AT, SANRT, AVNRT atypical
28. s
AVNRT AVRT
Incidence Most common Less than AVNRT
sex female males
Pathway Slow-fast,
Ventricles not required for
activation
Accesory
Ventricles required for
activation
Activation Simultaneous activation Sequential activation
Rate <200 >200
P-wave Burried in QRS Will be seen after QRS
Pseudo-r,pseudo-s,pseudo-q present absent
RP-interval <80msec >80msec
ST-T changes Less common more
ST elevation in aVR lesss more
Notch in aVL more less
QRS alternans Rare common
Abberancy Rare common
BBB Doesnot alter rate Alters rate(coumel’s law)
AV block Possible Not possible in its presence
30. • The slow pathway (alpha): a slowly-conducting pathway with
a short refractory period.
• The fast pathway (beta): a rapidly-conducting pathway with a
long refractory period.
AVNRT
31.
32. Presence of a narrow complex tachycardia with regular R-R
intervals and no visible p waves.
P wave are buried in the QRS complexes –simultaneous
activation of atria and ventricles – most common presentation
of AVNRT –66%.
If not synchronous –pseudo s wavein inferior leads ,pseudo r’
wavein lead V1---30%cases .
P waves are retrograde and are inverted in leads II,III,AVF
P wavemay be farther awayfrom QRS complex distorting the
ST segment ---AVNRT ,mostly AVRT.
37. What are “Pre-excitation syndromes” ?
• Term coined by Ohnell
• First described in 1930 by Louis Wolff, John Parkinson and Paul Dudley
White.
• A group of ECG and Electrophysiological abnormalities in which
– The atrial impulses are conducted partly or completely, PREMATURELY, to
the ventricles via a mechanism other than the normal AV-node
– Associated with a wide array of tachycardias with both normal QRS and
prolonged QRS durations
39. • “Manifest Pathways”
–Per se, WPW refers to patients with
pre-excitation in ECG + symptomatic
episodes of tachycardia.
• “Concealed Pathways”
- Patients with Accessory Pathways, but no
pre-excitation .
- Pathways may become manifest during
episodes of tachycardia
40. WPW
• PR interval <120ms
• Delta wave – slurring slow rise of
initial portion of the QRS
• QRS prolongation >120ms
• ST Segment and T wave discordant
changes – i.e. in the opposite
direction to the major component
of the QRS complex
• Pseudo-infarction pattern can be
seen in up to 70% of patients – due
to negatively deflected delta waves
in the inferior / anterior leads
(“pseudo-Q waves”), or as a
prominent R wave in V1-3
(mimicking posterior infarction).
WPW in sinus rhythm
42. Two types
Orthodromic
Antidromic
Antidromic is wide complex tachycardia
In NSR detected by delta wave.
Can ppt into AF and VF on use of AV nodal blockers
MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe.
CONCEALED WPW syndrome – no delta wave .less risk of
AF
43. Typical – RP interval <PR interval
RP interval >80 millisec
Atypical –RP interval >PR interval
Concealed bypass tract – only retrograde conduction
Manifest bypass tract– both anterograde and
retrograde.
Electrical alternans –the amplitude of QRS
complexes varies by 5 mm alternatively.
Rate related BBB occuring and the rate of tachycardia
is decreasing –then the bypass tract is on the same
side of the block.
62. P wave morphology changes.
PR interval > 0.12 sec .
Second,third degree AV block can occur.
Tachycardia terminates with a qrs complex ..
Right atrial origin– p wave inverted in V1.
If biphasic in V1—initially positive then negative.
Upright in lead AVL
Opposite if of left atrial origin
Superior origin –upright p waves in inferior leads
Inferior origin –p waves are inverted in inferior leads.
63.
64.
65. At least three consequtive p waves with different morphologies
with a rate >100 bpm to be present.
Isoelectric baseline between p waves.
Also called as choatic atrial tachycardia
Mostly seen in COPD ,electrolyte abn,theophylline
Rate usually does not exceed 130-140 bpm.
69. Non paroxysmal – accelerated junctional rhythm
Rate < 100 bpm Usually junctional node 40-60 bpm
Paroxysmal or focal junctional tachycardia is
rare – automaticity.
110-250bpm.
P waves may be before or after QRS complex
Infrequent and nonsustained episodes –no treatment
Acute termination of SVT and establish the mechanism
of SVT in case of acute setting.
Long term goal is abolishing the arryhthmia substrate.
Precipitating factors – electrolyte
imbalance,hypoxia,ischemia,hyperthyroidism to be
sought out.
73. A12 lead ECG during tachycardia and NSR.
No delay in therapy if the mechanism of SVT is not
known.
Perform CAROTID SINUS MASSAGE,or give6mg
bolus adenosine.
In case of severe hemodynamic compromise a
synchronised cardioversion to be given.
74. Check for carotid bruit before massage.
At the level of cricoid cartilage,at the angle of mandible
the carotid sinus is situated.
Gentle pressure is applied over the carotid sinus for 5
-10 seconds.
ECG recording to be present.
In case of no response – try on the other side.
Simultaneous pressure not to be applied both sides.
Alternative manuevres are valsalva,gagreflex,ice water
pouring over the face.
75. If SVT is suspected to be AVnode dependent – drug
of choice is adenosine and CCBs verapamil and
diltiazem.
Useful for sustained cases of AV node independent
tachycardias.
But digoxin,BBs,CCBs better control of ventricular
response in atrial tachycardias
Class I agents to be combined withAV nodal blocking
drugs – to eliminate 1:1 conduction of atrial to
ventricles.
84. In whom recurrences areinfrequent.
But sustained.well tolerated hemodynamically.
Patients who have had only asingle episode of SVT..
100-200mg of flecainide at the onset of SVTis areasonable
approach…until he reaches the hospital.
40-160 mg verapamil –without preexcitation,
Betablockers
Propafenone 150-450 mg.
80%casesinterrupted with acombination of CCBandBBin2
hrs…
85. Frequency and severity ofepisodes.
LVF
Costbenefits of radiofrequency ablation over the
pharmacotherapy .
Pharmacotherapy isconsidered in patients who defer
catheter ablation,whom in which ablation failed,or
carries arisk ofAVblock.
Multifocal atrialtachycardia
Trial anderror
Accessory pathway –classIa,Ic,III
AVnode blockingdrugs
Young patients –Iadrugs
ClassI agents LVD<35%notused.
Longterm
treatment
Membrane
activeAAD
Catheter
ablation
Curativesurgery
Antitachycardia
pacing
86. not to be used in bronchospastic pulmonary
disease.
Adenosine precipitates asthma
Given rapidly in 1-2 sec.
If given by peripheral vein uplift the arm..
Max dose is 30 mg
6- 12-12 mg
Terminates AVNRT .AFL with 2:1 block
Potentiated by dipyradimole,carbamazepine –
87. Calcium channel blockers,beta blockers
,digoxin are the next drugs to be used if
not responded to adenosine
Usually 60 % cases respond to a dose of 6
mg and 95 % cases at 12 mg.
Type 1 a AAD, 1c,iii,AMIODARONE in
refractory cases.
Beta blockers not to used IV in heart
failure.
88. Several multipolar catheters are introduced
High right atrium ,bundle of his ,RVapex,Coronary
sinus.
Radiofrequency is delivered at the site of earlier
activation
Success is defined by elimination of the tachycardia or
loss of pre excitation.
90-98% success in AV node dependent
60-80% in case of AV node independent.
Cryoablation more useful…
90. Temporary role in caseof digoxintoxicity.
Permanent in caseof long termcontrol
Toterminate thetachycardia
Revert into sinusrhythm
Prevent the occurrence.
Overdrive suppression
RFinduced atrial pacing areused
No role of surgery presently in PSVTrx.
91. ACUTE LONGTERM
PHYSIOLOGICAL rest ,sedation valsalva
Valsalva maneuvre Carotid sinusmassage
Carotid sinusmassage
PHARAMACOLOGICAL vagomimmetic Suppresstriggering
arrhythmias
Direct effect onAVnode Change propertiesof
reentrant pathways
SlowVR ControlVR
CATHETERABLATION
SURGERY
Ablation or sectioning of
reentrant pathway
ELECTRONICDEVICES Temp.pacing
cardioversio
n
Permanent pacemaker
Antitachycardiapacing
92. Rxof PSVT given for patient comfort except
in IHD,MS
When the QRS complex is wide and VT is
mistaken as SVT with ABERRANT conduction
IV verapamil – not recommended decreases
BP.
If DC cardioversion to be avoided because of
possible adverse response to digitalis adm
…pacing Rt atrium and ventricle via temp
pacing.
In WPW syndrome avoid
93. • Rx of ectopic atrial
tachycardia – consider
digitalis toxicity,chronic lung disease,metabolic
abn,electrolyte abnormalities,acute MI ----
temporary pacing.
Unsuccessful is EC
Removal or reversal of inciting factor
Surgical excision of focus.
Rx of MAT –chronic lung
disease,metabolic,rare is digitlais toxicity ---
CCBS,BBs ..no role of cardioversion,devices
94. In case of WPW syndrome
symptomatic concealed or
manifested ..and evidence of
preexcitation on NSR …send
the patient for catheter
ablation…
95. 1. carotid sinus pressure
2.IV adenosine.
3.long term treatment depends upon episodes.
4.any underlying abnormality to be checked
for.
5.definitive etiology only knon by EP study.
6.95% cases respond to RF ablation.
7.much less complications with cryoablation.
8.in case if SVT recurrs after ablation –opt
116. 1.Coexisting Double Tachycardias
May not be identified during noninvasive testing ..needs EP
study.
Ex—typicalAVNRT andAT.
Concentric –eccentric –concentric.
AVNRT –both APC,VPC
AT onlyAPC
2.Pseudo AF- infrequent presentation of PSVT.
Occurs during onset and termination of tahcycardia.
Multiple accessory AV pathways.
In young who haveAF without other risk factors.
5%of AVNRT.
Group beating is seen
ATRIAL TACHYCARDIA – FOCAL, MACRO RE ENTRANT, SINOATRIAL REENTRY
ATRIAL FLUTTER- RT- CLOCKWISE , COUNTER CLOCKWISE LT- MITRAL RE ENTRY, SCAR MEDIATED,PULMONARY VEIN
ALMOST ALL IRREGULAR TACHYS ARE AV NOT INDEPENDENT